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Updated: Jul 5, 2025
Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
Published on: September 25, 2019
5-FU promotes HBV replication through oxidative stress-induced autophagy dysfunction.
Jing Yang1, Luyan Zheng1, Zhenggang Yang1
1State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Chemotherapy for Hepatitis B virus (HBV)-related liver cancer can trigger HBV reactivation. This study reveals that 5-fluorouracil (5-FU) promotes HBV replication by disrupting autophagy via reactive oxygen species (ROS), offering new therapeutic targets.
Area of Science:
- Hepatology
- Oncology
- Virology
Background:
- Hepatitis B virus (HBV) reactivation is a significant clinical challenge during chemotherapy for HBV-related hepatocellular carcinoma (HCC).
- The precise mechanisms driving chemotherapy-associated HBV reactivation remain incompletely understood, impeding the development of effective treatments for HBV-related HCC.
Conclusions:
- Reactive oxygen species (ROS)-induced autophagosome formation and impaired autophagic degradation are critical mechanisms in 5-FU-induced HBV reactivation.
- Targeting ROS and autophagy pathways may offer novel strategies to prevent HBV reactivation during chemotherapy for HBV-related HCC.
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